Review Volume 16, Issue 11 pp 10165—10196

Figure 1. The therapeutic strategies targeting macrophages have been noticeable in recent years. Single application and combined application with traditional drug therapy have great potential. According to their mechanisms, they are mainly divided into the following categories. Reducing the recruitment of TAMs includes the use of αCSF-1, αCSF-1R, TD-92 (CSF-1R inhibitor), carlumab (αCCR2), maraviroc (CCR5 inhibitor), OLA-PEG (CXCL12 inhibitor), and AMD3100 (CXCR4 inhibitor). Reprogramming TAMs to the M2-like phenotype includes the use of TG100-115 (PI3Kγ inhibitor), poly (I:C) (TLR3 agonist), resiquimod (TLR7/8 agonist), R848 (TLR7/8 agonist), αCD40, and simvastation. TAMs inhibit the T-cell-induced immune response through PD-1/PD-L1, PGE2, IL-10, and TGF-β. The use of αPD-1, αPD-L1, and macrophage targeted therapy may activate T-cell-induced immune response. Blocking the “don’t eat me” signal includes the use of αCD24, magrolimab (αCD47), Rx-001 (both SIRP-α and CD47 inhibitor), and siRNAs against JMJD1A.